The present invention generally relates to implantable cardiac stimulation devices, e.g., pacemakers or implantable cardioverter defibrillators (ICDs). The present invention more particularly relates to an implantable cardiac stimulation device and method which provide pacing of a heart in different modalities while assisting in the treatment of atrial arrhythmias by prolonging atrial refractoriness of the heart.
Atrial arrhythmias such as paroxysmal atrial fibrillation and flutter are very common arrhythmias. Such arrhythmias are present in a large percentage of the bradycardia pacemaker patient population. For these patients, pacemaker therapy could become a primary indication for treatment of the disorder.
The prolongation of atrial refractoriness is known to reduce the likelihood of atrial arrhythmias in some patients. Certain drugs, such as amiodarone or beta-blockers, like sotalol, help to maintain sinus rhythm by prolonging atrial refractoriness and thus act to reduce atrial arrhythmias in some patients. Other drugs help slow the ventricular rate once atrial fibrillation has occurred. These drugs reduce ventricular rate by AV nodal inhibition. These include verapamil, diltiazem, beta-blockers, and/or digoxin. However, drugs can cause side effects and many patients are resistant to drug therapy.
It would therefore be desirable to have some means other than the ingestion of drugs available to this patient population for prolonging atrial refractoriness. To that end, preemptive electrical stimulation of the atrium is known to prevent atrial arrhythmias in some patients. The present invention addresses these issues in the form of an implantable cardiac stimulation device capable of pacing the heart of a patient in single or dual chamber modalities while pacing the atria in an improved manner which assists in prolonging atrial refractoriness and treating atrial arrhythmias. Furthermore, the present invention provides therapeutic benefit to patients with hypertension, heart failure, acute myocardial infarction and other disorders as described below.
Others have sought to prevent the onset of atrial arrhythmias with pacing. For example, U.S. Pat. No. 5,403,356 to Hill uses at least two electrode pairs with one electrode pair being used to detect a depolarization at a one site, e.g., the high right atrium and detection triggers stimulation to the triangle of Koch or a site of prolonged effective refractory period. The triggered stimulation occurs synchronous with the detection or following a short time delay of less than 50 ms. This short time delay is used to prevent stimulation during the vulnerable period in the atrium and thus avoids precipitating atrial arrhythmias. Although stimulation at the triangle of Koch is intended to synchronize the atrium and the refractory periods in the atrium, it is not intended to act to prolong atrial refractory periods. Furthermore, this approach requires implantation of multiple atrial leads and thus complicates the process of administering therapy.
Atrial tachyarrhythmias are often preceded by at least one atrial premature beat that spontaneously originates from an ectopic site in the atrium. Mehra has proposed in U.S. Pat. No. 5,683,429 using burst pacing at multiple sites immediately after an atrial premature beat to prevent a reentry event precipitated by the atrial premature beat. Mehra also teaches that there may be an unspecified time delay between the atrial premature beat and the burst of pacing. Although this algorithm was intended to block reentry as a result of atrial premature beats, it does not act to prevent atrial premature beats and the potentially ensuing atrial arrhythmias.
The present invention further acts to prevent atrial premature beats by making the ectopic foci responsible for the atrial premature beat refractory and thus incapable of spontaneously depolarizing.
Furthermore, the present invention has the effect of prolonging the interval between the pacing atrial events and succeeding spontaneous native atrial depolarizations. This actually makes it possible to reduce the hemodynamically effective cardiac rate to a rate lower than the native rate which is useful for regulating blood pressure. This will benefit patients with essential hypertension, and patients with heart failure in whom reducing blood pressure reduces cardiac work and reduces ventricular wall tension. Reducing the ventricular wall tension allows the heart to assume a smaller more normal geometry and thus allows for more effective contraction.
Slowing the hemodynamically effective rate below the native rate has significant benefits to patients with coronary heart disease. Perfusion of the myocardium takes place during diastole and thus slowing the rate increases the diastolic interval and thus allows more time for perfusion of ischemic cardiac tissue.
A further therapeutic application of the present invention is in the treatment of patients with diastolic dysfunction. These patients have hypertrophied hearts with reduced compliance. Reducing the effective hemodynamic rate has the benefit of allowing more time for filling the relatively stiff, incompliant ventricles and thus enhances stroke volume and cardiac performance.
Other therapeutic benefits are likely to become apparent with extensive practice of the present invention.
The invention therefore provides an implantable cardiac stimulation device, e.g., a pacemaker or ICD, including generating means for delivering pacing pulses to an atrium of a heart and control means coupled to the generating means for causing the generating means to deliver a primary pacing pulse to the atrium and causing the generating means to deliver a secondary pacing pulse to the atrium a delay time after the delivery of the primary pacing pulse.
In accordance with further aspects of the present invention, the implantable cardiac stimulation device may further include a detector that detects atrial activations of the heart, wherein the generator control inhibits the generator from providing the primary pacing pulse when an atrial activation is detected during an escape interval and wherein the generator control further causes the generator to deliver the secondary pacing pulse to the atrium the delay time after an atrial activation is detected during the escape interval.
In accordance with still further aspects of the present invention, the implantable cardiac stimulation device may further include an AV delay timer that times an AV delay interval responsive to the delivery of a primary pacing pulse or the detection of an atrial activation within the escape interval, and a second generator responsive to the AV delay timer that provides a ventricular pacing pulse at the end of the AV delay interval.
In accordance with still further aspects of the present invention, the implantable cardiac stimulation device may further include a ventricular detector that detects ventricular activations of the heart and a ventricular inhibitor that inhibits the second generator when a ventricular activation is detected during the AV delay interval.
The present invention still further provides a method of pacing atria of a heart. The method includes the steps of delivering a primary pacing pulse to one of the atria of the heart, timing a delay time period following the delivery of the primary pacing pulse, and delivering a secondary pacing pulse to the one of the atria at the end of the delay time period.
The present invention also discloses a means to automatically establish the delay timing of delivery of the secondary atrial pulse. The advantage of automated adjustment of the delivery of the secondary pacing pulse is that there is no necessity to manually adjust the interval. Additionally, if there are physiologic changes to the patients heart that would necessitate adjustment of the delay it will be automatically performed by the device thus automatically optimizing therapy.